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* Department of Internal Medicine,
VA Research Service,
Molecular Microbiology & Immunology, and
Pathology, University of Missouri, School of Medicine, Columbia, Missouri
Correspondence: Dr. Helen B. Mullen, Division of Immunology & Rheumatology, University of Missouri, M450 Medical Sciences, Columbia, MO 65212. E-mail: mullenh{at}health.missouri.edu
This study was initiated to identify and characterize thyroid fibrosis
in a murine model of granulomatous experimental autoimmune thyroiditis
(G-EAT) and determine if TGF-ß1 might be involved in fibrosis. G-EAT
was induced by transfer of mouse thyroglobulin-sensitized spleen cells
activated in vitro with thyroglobulin, anti-IL-2R, and
IL-12. There was almost complete destruction of thyroid follicles,
leading to fibrosis of the gland and reduced serum T4 levels. Fibrosis
was confirmed by staining for collagen and 
smooth-muscle actin, a
marker of myofibroblasts. Kinetic studies characterized the onset and
development of thyroid fibrosis. TGF-ß1 was increased at mRNA and
protein levels, and expression of TGF-ß1 protein paralleled G-EAT
severity. Comparison of staining patterns showed that TGF-ß1 was
expressed in areas of myofibroblast and collagen accumulation, implying
that TGF-ß1 may play a role in fibrosis in G-EAT. Further studies
demonstrated that myofibroblasts, macrophages, and thyrocytes
contributed to TGF-ß1 production. This provides an excellent model to
study the mechanisms of fibrosis associated with autoimmune
damage.
Key Words: autoimmune disease • myofibroblasts • TGF-ß1
This article has been cited by other articles:
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